Abstract
The acute subcutaneous toxicity of isoprenaline was found to depend on body temperature. Since isoprenaline increases both heat production and heat loss, its effect on body temperature was influenced by the thermoregulatory capacity of an animal. An increased hyperthermic action of the drug following a rise in ambient temperature by 4° was associated with 10 times increased toxicity. Increased heat production capacity following cold acclimatisation resulted in increased toxicity at room temperature but no more than in a cold environment. The higher body weight to body surface ratio in bigger rats diminished the isoprenaline–induced hypothermia. On the other hand, hypothermia reduced tachycardia and pulse pressure responses to isoprenaline. However, cardiomegaly and myocardial lesions produced by small and repeated doses of isoprenaline (5 mg/kg daily for 4 days) were independent of whether the animals were hypo– or hyperthermic after the injections. In addition, the extent of cardiac enlargement was as great in small rats as in the larger rats. It is concluded that hypothermia protects the heart from acute failure but not from hypoxia, which may be the main reason for cardiomegaly and myocardial lesions after isoprenaline.